June 16, 2025 • 19 mins
🧑⚕️ FREE MSRA PODCAST – Lichen Planus: Mastering the Purple Pruritic Rash
🎯 A deep dive into lichen planus, one of the MSRA’s favourite inflammatory skin conditions—covering core facts, memorable mnemonics, diagnosis, management, and red flags.
Key Learning Points
🔍 Definition
• Lichen planus is a chronic, immune-mediated inflammatory disorder affecting the skin, mucous membranes, hair, and nails.
• Classic description: the “6 Ps”—Pruritic, Purple, Polygonal, Planar, Papules, and Plaques.
• Wickham striae: fine, white, lacy lines seen on the surface of papules and in the mouth.
💡 Causes & Risk Factors
• Precise cause unknown, but believed to be T-cell mediated autoimmunity.
• Strong associations: Hepatitis C infection (particularly oral LP), certain medications (e.g., NSAIDs, beta-blockers, thiazides), stress, and family history.
🧬 Pathophysiology
• CD8+ T-cell attack on basal keratinocytes in the skin and mucous membranes
• Triggers: drugs, viral infections, genetic susceptibility
🩺 Clinical Features
• Itchy, purple, flat-topped, polygonal papules—flexor wrists, forearms, shins, lumbar region
• Wickham striae: white, lacy lines (esp. in oral or genital mucosa)
• Oral/genital ulcers may be painful and chronic
• Nail changes: ridging, thinning, pterygium, or loss
• Scalp involvement: lichen planopilaris—patchy, permanent hair loss
• Post-inflammatory hyperpigmentation is common after lesions heal
📌 Mnemonic: The 6 Ps
• Pruritic (itchy)
• Purple
• Polygonal
• Planar
• Papules
• Plaques
📝 Differential Diagnoses
• Psoriasis
• Eczema
• Lichenoid drug eruptions
• Chronic eczema (simplex)
• Oral: Thrush, leukoplakia, oral lichenoid reaction
🔬 Diagnosis
• Clinical appearance often sufficient
• Skin or mucosal biopsy—shows “sawtooth” lymphocytic infiltrate, hypergranulosis, basal cell degeneration
• Test for hepatitis C if risk factors or oral involvement
💊 Management
• Remove any causative drug if identified
• First line: potent topical corticosteroids (with or without occlusion)
• For oral/genital LP: topical steroids (mouthwashes, pastes), local anaesthetics
• Widespread, severe, or resistant disease: systemic corticosteroids, immunosuppressants (azathioprine, mycophenolate), retinoids, phototherapy (UVB/PUVA)
• Antihistamines for pruritus
• Regular monitoring for oral/genital LP (risk of squamous cell carcinoma)
📈 Prognosis
• Cutaneous LP is often self-limiting (resolves in 1–2 years), but recurrences may occur
• Oral/genital LP: chronic, relapsing course, higher risk of persistent symptoms and malignant change
• Watch for post-inflammatory pigmentation, scarring (scalp/nails), or persistent discomfort
⚠️ Complications
• Malignant transformation (especially oral/genital LP; ~1% lifetime risk—higher with smoking, Hep C)
• Scarring, particularly on the scalp (permanent alopecia) or nails
• Persistent pain, ulceration, or impaired quality of life
📎 More MSRA Revision for Lichen Planus:
📝 Revision Notes: https://www.passthemsra.com/topic/lichen-planus-revision-notes/
💬 Flashcards: https://www.passthemsra.com/topic/lichen-planus-flashcards/
🧠 Accordion Q&A: .css-j9qmi7{display:-webkit-box;display:-webkit-flex;display:-ms-flexbox;display:flex;-webkit-flex-direction:row;-ms-flex-direction:row;flex-direction:row;font-weight:700;margin-bottom:1rem;margin-top:2.8rem;width:100%;-webkit-box-pack:start;-ms-flex-pack:start;-webkit-justify-content:start;justify-content:start;padding-left:5rem;}@media only screen and (max-width: 599px){.css-j9qmi7{padding-left:0;-webkit-box-pack:center;-ms-flex-pack:center;-webkit-justify-content:center;justify-content:center;}}.css-j9qmi7 svg{fill:#27292D;}.css-j9qmi7 .eagfbvw0{-webkit-align-items:center;-webkit-box-align:center;-ms-flex-align:center;align-items:center;color:#27292D;}Mark as PlayedTranscript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
OK, let's dive in. Imagine you're prepping for the
MSRA, maybe reviewing some derm cases.
Or perhaps you're in clinic and a patient comes in, they've got
these really itchy, like purple bumps, raised bumps on their
wrists, maybe their shins. OK, yeah, classic spots.
You look closer and there are these faint sort of delicate
(00:20):
white lines across some of them,and then they mention, oh, and
I've got the sore bit inside my mouth kind of white.
Makes eating spicy food a nightmare.
Does that really need Belle? Something that might, you know,
pop up on the exam. That whole picture, it should
definitely make you think like in plaintiffs straight away.
Spot on. And that's our focus today.
We're doing a deep dive into Lincoln plaintiffs using, well,
(00:42):
the kind of high yield info you really need for MSRA revision.
Yeah, it's a core topic. So the plan is we'll break it
down, get the essentials sorted,what it is, why it happens, what
it actually looks like and crucially, how you manage it,
what to watch out for. Basically a focused revision
session. Lichen planus pops up quite a
bit different scenarios so knowing the key features is
(01:03):
vital. It's inflammatory, can hit
multiple spots, you just have torecognise it.
So let's start right at the beginning.
What actually is lichen planus fundamentally?
OK, so at its heart, it's a chronic inflammatory condition.
We mostly think skin, right? But it's really important to
remember it often hits the mucous membranes too, like a
mouth. Exactly.
Mouth genitals, and sometimes, though less commonly, it can
(01:27):
affect hair and nails as well. And what's the classic
description if you had to paint a picture well?
Traditionally people talk about the six PS but maybe more
helpfully for spotting it, thinkpruritic.
So really itchy. OK, polygonal multi sided
shapes, not just round right papioles which are small bumps
and plaques larger flat topped areas.
Right itchy polygonal bumps and plaques colour.
(01:50):
Often purplish or violacious is the term you'll see.
And those white lines you mentioned, That's Wickham stri a
really a key feature. Looks like a Lacy pattern on the
surface. Wickham stri a got it.
So itchy purple polygonal Azesians, often with these white
lines. Where do they like to hang out?
Flexor surfaces are classic, so inside of the wrists, forearms,
(02:12):
lower legs are common spots. But like we said, mucous
membranes are involved in a lot of cases, mouth especially.
And genitals, too. Yes, definitely.
And the hair and nails. You mentioned those earlier,
yeah. Less common?
Uh huh, but imortant on the scalp.
It's called Lakin plantipolaris,and that's serious because it
can cause scarring, permanent hair loss.
(02:33):
Oh. Right Nail changes can be things
like ridges, thinning, splitting, just generally
looking unhealthy, dystrophic, so you need to check everywhere
if you suspect it. Understood.
And what's going on underneath? Is it just like a random rash?
No, no. It's more specific than that.
We don't know the exact trigger but we understand it's AT cell
mediated immune thing. So the body's own immune system.
Exactly. Certain T cells are involved in
(02:56):
driving that inflammation and causing the damage you see.
Is it common? It's not rare.
Estimates are around one in 100 people globally, maybe 1 to 2%
here in the UK. Typically hits adults usually
between 30 and 60 years old. OK.
And are there other things linked to it?
Other conditions? Triggers.
Yes, absolutely. And these are really high yield
associations for the exam. Think autoimmune factors,
(03:18):
generally certain medications. Think which ones.
Things like beta blockers and SAis some diuretics,
antimalarials, gold salts, the list is quite long.
And importantly, viral infections, especially hepatitis
C. The Hep C link, I remember that.
Definitely remember that one, particularly for oral lichen
plainus. The association is quite strong.
(03:39):
Worth thinking about testing. OK, so inflammatory, distinct
look multiple sites immune driven linked to meds and hep C.
What's the usual course? Does it just go away?
The. Skin form cutaneous lichen
plainus. Often it's self limiting.
It might resolve on its own overmonths, maybe a year or two.
But the mucosa drain type, especially if it's erosive,
meaning causing sores or ulcers in the mouth or genitals, that
(04:03):
tends to be much more persistent, and this is crucial.
It carries a small but definite risk of malignant change over
time. OK, that cancer risk is
definitely something we need to circle back to big time.
But first let's dig into the whya bit more aetiology risk
factors, you said T cell mediated, but what actually sets
that off? Yeah.
So the exact initial spark, still a bit of a mystery, but
(04:26):
the general idea is it's an autoimmune type response where
the immune system gets misdirected against the body's
own skin or mucosal cells. What might nudge it in that
direction? What are the potential triggers
or things that make it worse? Well, the source of point to a
few things. There might be a genetic
predisposition. Sometimes it runs in families.
Viral infections like we said, Hep C is the main one to flag
(04:48):
those medications. We listed beta blockers, NSAI,
thiazides, antimalarials, gold and potentially allergens.
Maybe contact allergens like dental materials for oral LP or
other environmental factors. So if we list the actual risk
factors explicitly, what makes someone more likely to get it?
OK. Based on that, definitely a
(05:09):
family history having certain infections, especially hepatitis
C, exposure to those known trigger medications and
potentially exposure to certain allergens or environmental
triggers. Makes sense.
So we have the what and the potential why?
Now the how. Let's talk pathophysiology.
What's actually happening at thecellular level to create those
(05:29):
lesions? Right, this is where those T
cells come in. It's primarily CD 8 + T cells, a
specific type of immune cell. These cells target the basal
keratinocytes. Basal, meaning the bottom layer,
the foundation of the epidermis.Exactly.
Think of it like the skins foundation layer.
These CD 8 + T cells seem to recognise something on those
basal cells as foreign or abnormal and they attack them.
(05:50):
This happens in the skin and in mucous membranes.
So the body's own security forceattacking its own building
blocks. That's a good way to think about
it, yeah. And that attack releases
inflammatory signals, cytokines,which then 'cause all the
inflammation and the changes we see, the redness, the swelling,
the cell damage that leads to the papules and plaques.
And the trigger for that initialattack is still the unknown
(06:13):
part. Often, yes, though genetic
factors and those environmental triggers likely play a role in
making someone susceptible or setting it off.
OK, that helps visualise it. And this ties in nicely with
Histology, right? Which is super important for
tricky cases and exams. If you biopsy one of these
lesions, what are the classic microscopic findings?
(06:33):
Absolutely crucial. So under the microscope you're
looking for a few key things. First, a sawtooth appearance of
the REIT ridges. That's where the epidermis dips
down into the dermis. It looks jagged, not smooth.
Thought to you, it's got it. Second, a dense band like
infiltrate of lymphocytes, mainly those T cells clustered
right underneath the epidermis along that junction band of.
Lymphocytes. 3rd signs of damageto that basal cell layer.
(06:56):
We call it vacuular alteration or degeneration.
Yeah, basically the cells being attacked.
Right damage at the base. And 4th you often see
hyperkeratosis, which is thickening of the top layer of
skin and hypergranulosis, thickening of the granular layer
just below that. And does that granular layer
thickening link to anything we see clinically?
It's thought to that thickened granular layer is believed to be
(07:18):
what causes the appearance of Wickham's Tria.
Those white lines. So thick granular layer
microscopically links to white lines clinically.
Nice connection. Anything else on the Histology
report? Yes.
Sometimes you'll see these little pink blobs called SAVAT
bodies which are dead keratinocytes and direct
immunofluorescence or DIF can behelpful too.
What does DI show? It often shows deposits of
(07:41):
immunoglobulins, particularly IGN and fibrinogen, in a shaggy
pattern along that dermal epidermal junction.
OK, so key Histology buzzwords, sawtooth root ridges, band like
lymphocytic infiltrate, basal cell damage, hydrogranulosis
linked to Stryi and maybe IGN onDIFSBBHI, something like that.
(08:01):
Whatever works for you, Mimonicsare definitely helpful here.
OK. Speaking of things that might
look similar, differential diagnosis, what else could
present like lichen planus and potentially trip you up?
Good question. Always need to consider the
mimics for skin lesions you think about psoriasis, eczema,
maybe like a simplex chronicus which is from chronic scratching
(08:22):
and definitely drug reactions, specifically lycanoid drug
eruptions. Which look very similar.
Almost identical sometimes. That's why the medication
history is so vital. If they started a new beta
blocker with Thiazide recently, that's a big clue right?
And in the mouth. Oral differentials include
thrush, oral Candidiasis, but remember that usually wipes off
other oral lycanoid reactions, maybe from dental fillings and
(08:45):
importantly leukoplachia which is another white patch but can
also be precancerous. So differentiating is key.
Biopsy is often needed for oral lesions if unsure.
OK. And just thinking broadly, any
other conditions that sometimes get confused with LP from the
wider list? Yeah, things like cutaneous
graft versus host disease in transplant patients can look
(09:05):
similar. Discoid lupus erythropasias can
sometimes present with lesions that mimic LP and lichen
sclerosis, especially on the generals can overlap or be
confused, so keep a broad mind if it's not textbook.
Definitely. OK, let's zoom out again to the
big picture epidemiology. How common is it?
Who gets it? We mentioned the UK prevalence
(09:26):
around one 2%. It's mostly a condition of
middle age. Think 30s to 60s typically.
Yeah, and male versus female. Overall pretty similar for skin
LP, but for oral like and plaintiffs specifically it does
seem to be a bit more common in women.
Maybe a global ratio around 1 to1.5 female to male?
Interesting. And those associations again
globally? Yeah, the link with hepatitis C
(09:47):
is seen worldwide and also associations with hepatitis B
and primary biliary cirrhosis are noted in wider studies.
OK, prevalent enough to see middle-aged adults, maybe
slightly more oral LP in women and those important liver
disease connections. Right?
Let's really nail the clinical features.
Now back in the room with the patient.
What absolutely must you recognise?
OK consolidation time, cutaneousLP, itchy, purple, vilacious,
(10:13):
polygonal flat topped papules and plaques.
Think wrists, forearms, lower legs, ankles but can be
anywhere. Look hard for Wickham.
Striate those fine white lines. Sometimes easier to see if you
put a drop of oil or water on the lesion.
Good tip. And remember, after they heal
they can leave brown marks post inflammatory hyperpigmentation,
(10:34):
especially in darker skin. OK.
And mucous membranes? How common again?
And what's the look? Super common for oral
involvement. Up to 50% of people with skin LP
have it and some only have oral LP.
Look inside the cheeks, glucose,mucosa, the tongue, gums.
You'll often see white Lacy patches.
Maybe Wickham's dry again? Are they always sore?
No, they can be asymptomatic butoften they are sore, especially
(10:55):
if they become erosive or ulcerated.
Looks like raw red areas, sometimes with white edges.
General involvement is similar. Can be very painful erosions.
How do you tell oral LP from Thresh quickly?
Thrush is usually creamy or maybe look like cottage cheese
and crucially it should wipe offleaving a red base.
Lake and Planus is usually flatter, lacier and doesn't wipe
off. Got it.
Nail and scalp. Quick recap.
(11:16):
Males in up to 10%. Look for longitudinal ridges,
thinning, splitting, maybe terradium where the cuticle goes
forward. Scalp.
Lincoln plantipolaris, Patchy hair loss, redness, scaling
around follicles leading to scarring.
Alopecia. Less common, but important not
to miss. OK, so key features rundown
itchy purple polygonal rash wrists, legs, flexors, genitals
(11:39):
Wickham striae look for them Oral involvement in 50% Check
the mouth potential nail and scalp changes Diagnosis often
clinical. Spot on and always factor in
risk factors, Hep C, stress, newmeds, allergies and think about
those lycanoid drug mimics. Perfect mini case time.
Let's say a 55 year old man presents with intensely itchy
(11:59):
purple bumps on his wrist. You see faint white lines.
He also mentions a sore patch inside his cheek when he eats
salty crisps. What's jumping out at you?
That's screaming like in plaintiffs.
You've got the Puritic violations, polygonal papules on
a classic site, wrists with Wickhamstrae, plus symptomatic
oral involvement. Textbook presentation.
Really. Excellent.
Now what if it's not so textbook?
(12:20):
What investigations might you actually order?
Well, if it looks classic, you often don't need investigations.
Diagnosis is clinical, but if it's atypical or you need to
rule out something more sinisterlike malignancy in an oral
lesion or differentiate from a mimic, then a biopsy is your go
to. A punch biopsy.
Usually, yes, a punch biopsy sent for histopathology and we
(12:43):
know what they're looking for. Sawtooth band like infiltrate,
basal damage, hypergranulosis. Exactly, and you might ask for
direct immunofluorescence DIF ona separate biopsy sample taken
from near lesion looking for those IGN deposits.
OK. Any other tests?
Well, for persistent oral LP, especially if you suspect a link
to amalgam fillings, patch testing could be considered to
(13:05):
look for contact allergy, right?And given the strong
association, definitely considerhepatitis C testing,
particularly if the oral LP is erosive or if the patient has
any risk factors for Hep C. So investigations mainly for
confirmation and tricky cases orchecking for associations like
hep C clinical picture is king usually, right?
Let's talk management. How do we actually help these
(13:26):
patients? It really depends.
For mild skin LP that isn't too bothersome it might resolve on
its own so just reassurance might be needed.
But if it's itchy, widespread, or affecting mucous membranes
causing symptoms, then treatmentis usually warranted.
First step if you suspect a drugtrigger.
Stop the drug. If it's a lycanoid drug
eruption, removing the trigger is the most important step and
(13:48):
can lead to resolution. OK.
For itchy skin lesions, what's the first line?
Potent or super potent topical corticosteroids.
That's the mainstay creams or ointments applied directly to
the lesions. How do they help?
They reduce the inflammation andtherefore the itch and help the
lesions clear faster. For really thick stubborn
lesions, hypertrophic LP, sometimes applying the steroid
(14:10):
under occlusion like cling film overnight can boost its effect.
Antihistamines can help with theitch symptomatically too.
And for the mouth, oral LP. Again, topical steroids are
first line for symptomatic oral LP.
These come as mouthwashes, sprays or pastes that stick to
the lining of the mouth. Things like benzi tapping,
mouthwash or spray can also helpsoothe soreness.
(14:31):
What if topicals aren't cutting it or the disease is really
widespread or severe? Then you need to step up to
systemic treatment. Often this means a course of
oral corticosteroids like Prednisolone, usually for
several weeks, then slowly tapered down.
Any other options beyond steroids?
Yes, for difficult or persistentcases.
Other options include immunosuppressants like
(14:52):
azathioprine or mycophenolitma. Fatal.
Sometimes oral retinoids like acetretin are used.
Hydroxychloroquine is another one mentioned and phototherapy.
Light treatment. Exactly.
Narrowband UVB or Puva Soarland plus UVA Light can be very
effective for widespread itchy cutaneous lichen planus that
(15:12):
hasn't responded well to topicals.
OK, so summarising management stop triggers if suspected first
line for skin oral is potent. Topical steroids maybe
intralesional steroids for thicklesions step up to oral
steroids, other immunosuppressants, retinoids or
phototherapy for severe widespread refractory disease.
Symptomatic relief with antihistamines or anaesthetic
(15:33):
mouthwashes. That's a pretty good overview of
the treatment ladder. Right quick MSRA scenario on
management. A patient has widespread, very
itchy cutaneous lichen planus. Potent topical steroids haven't
really worked after a good few weeks.
What might be a reasonable next step?
Given it's widespread and not responding to topicals, you'd
think about systemic options. So starting a course of oral
(15:55):
corticosteroids or referring forphototherapy like UVB or PUVA
would be appropriate next steps to consider.
Makes sense nearly there prognosis.
What's the long term outlook? It's quite variable honestly.
Skin licking plant is often doesburnout, maybe within one two
years, but it can recur. And the mouth and other mucous
membranes. They tend to be much more
chronic. Erosive oral or genital OBP can
(16:17):
grumble on for many years with flare ups and periods of
remission. It's less likely to resolve
completely on its own. And even when the active bits
clear up. You can be left with changes
that post inflammatory hyperpigmentation.
The brown marks can persist for a long time and scarring is a
real issue, especially with lichen plantiplearis on the
scalp causing permanent hair loss or severe erosive disease
(16:39):
potentially causing scarring in the mouth or genitals.
So follow up is often needed. Which brings us neatly to
complications. What are the main problems or
long term issues we need to be aware of?
OK, this is super important for oral and genital LP.
The main issues are pain, soreness, ulceration.
This can make eating, drinking, speaking or sexual activity
(17:01):
really difficult and impact quality of life massively.
Can even lead to weight loss if eating is tough.
And the really serious one. The risk of malignant
transformation, specifically oral squamous cell carcinoma.
OSCC developing within the long standing, particularly erosive
oral lichen planus lesions. What's the kind of risk level
we're talking? The figures quoted are around a
(17:22):
1.1% risk over time. It's not huge, but it's
significant enough that regular oral cheques are recommended for
these patients. And does anything increase that
risk further? Yes, smoking and coexisting
hepatitis C infection seem to significantly increase the risk
of OSCC development in patients with oral LP, which again
highlights why asking about smoking and considering Hep C
(17:44):
testing is so important. Wow, so that really underlines
the need for monitoring any other complications?
Well, the persistent hyperpigmentation can be
cosmetically bothersome and rarely carcinoma can develop in
chronic vulval like in planus lesions too.
And of course, the underlying association with Hep C itself is
a complication to manage. So it's a condition that might
(18:06):
seem like just a rash sometimes,but particularly the oral and
genital forms need careful management and long term
surveillance because of that small but real risk of cancer,
especially if they smoke or haveHep C.
Exactly, you absolutely must check the mouth, ask about
symptoms there, consider risk factors and arrange follow up.
Particularly for erosive disease, it's not just about
(18:26):
treating the itch on the skin. That's a really crucial takeaway
message, right? We've covered a lot of ground,
the definition, the T cell cause, the classic 6 PS and
Wickham Strea, the key Histologymanagement from topicals to
systemics and those vital complications like OSCC risk.
Hopefully this deep dive gives you a solid high yield overview
for Leakin Planus when it comes up in your MSRA revision.
(18:49):
Yeah, connecting the pathology to the presentation and hitting
those high yield points for the exam was the goal.
Absolutely. Well, thanks for joining us for
this deep dive into Leakin Planus.
For more free MSRA revision resources, visit freem-sra.com
and for the full Premium Revision Toolkit, head to pass
them ssra.com.
OK, let's dive in. Imagine you're prepping for the
MSRA, maybe reviewing some derm cases.
Or perhaps you're in clinic and a patient comes in, they've got
these really itchy, like purple bumps, raised bumps on their
wrists, maybe their shins. OK, yeah, classic spots.
You look closer and there are these faint sort of delicate
(00:20):
white lines across some of them,and then they mention, oh, and
I've got the sore bit inside my mouth kind of white.
Makes eating spicy food a nightmare.
Does that really need Belle? Something that might, you know,
pop up on the exam. That whole picture, it should
definitely make you think like in plaintiffs straight away.
Spot on. And that's our focus today.
We're doing a deep dive into Lincoln plaintiffs using, well,
(00:42):
the kind of high yield info you really need for MSRA revision.
Yeah, it's a core topic. So the plan is we'll break it
down, get the essentials sorted,what it is, why it happens, what
it actually looks like and crucially, how you manage it,
what to watch out for. Basically a focused revision
session. Lichen planus pops up quite a
bit different scenarios so knowing the key features is
(01:03):
vital. It's inflammatory, can hit
multiple spots, you just have torecognise it.
So let's start right at the beginning.
What actually is lichen planus fundamentally?
OK, so at its heart, it's a chronic inflammatory condition.
We mostly think skin, right? But it's really important to
remember it often hits the mucous membranes too, like a
mouth. Exactly.
Mouth genitals, and sometimes, though less commonly, it can
(01:27):
affect hair and nails as well. And what's the classic
description if you had to paint a picture well?
Traditionally people talk about the six PS but maybe more
helpfully for spotting it, thinkpruritic.
So really itchy. OK, polygonal multi sided
shapes, not just round right papioles which are small bumps
and plaques larger flat topped areas.
Right itchy polygonal bumps and plaques colour.
(01:50):
Often purplish or violacious is the term you'll see.
And those white lines you mentioned, That's Wickham stri a
really a key feature. Looks like a Lacy pattern on the
surface. Wickham stri a got it.
So itchy purple polygonal Azesians, often with these white
lines. Where do they like to hang out?
Flexor surfaces are classic, so inside of the wrists, forearms,
(02:12):
lower legs are common spots. But like we said, mucous
membranes are involved in a lot of cases, mouth especially.
And genitals, too. Yes, definitely.
And the hair and nails. You mentioned those earlier,
yeah. Less common?
Uh huh, but imortant on the scalp.
It's called Lakin plantipolaris,and that's serious because it
can cause scarring, permanent hair loss.
(02:33):
Oh. Right Nail changes can be things
like ridges, thinning, splitting, just generally
looking unhealthy, dystrophic, so you need to check everywhere
if you suspect it. Understood.
And what's going on underneath? Is it just like a random rash?
No, no. It's more specific than that.
We don't know the exact trigger but we understand it's AT cell
mediated immune thing. So the body's own immune system.
Exactly. Certain T cells are involved in
(02:56):
driving that inflammation and causing the damage you see.
Is it common? It's not rare.
Estimates are around one in 100 people globally, maybe 1 to 2%
here in the UK. Typically hits adults usually
between 30 and 60 years old. OK.
And are there other things linked to it?
Other conditions? Triggers.
Yes, absolutely. And these are really high yield
associations for the exam. Think autoimmune factors,
(03:18):
generally certain medications. Think which ones.
Things like beta blockers and SAis some diuretics,
antimalarials, gold salts, the list is quite long.
And importantly, viral infections, especially hepatitis
C. The Hep C link, I remember that.
Definitely remember that one, particularly for oral lichen
plainus. The association is quite strong.
(03:39):
Worth thinking about testing. OK, so inflammatory, distinct
look multiple sites immune driven linked to meds and hep C.
What's the usual course? Does it just go away?
The. Skin form cutaneous lichen
plainus. Often it's self limiting.
It might resolve on its own overmonths, maybe a year or two.
But the mucosa drain type, especially if it's erosive,
meaning causing sores or ulcers in the mouth or genitals, that
(04:03):
tends to be much more persistent, and this is crucial.
It carries a small but definite risk of malignant change over
time. OK, that cancer risk is
definitely something we need to circle back to big time.
But first let's dig into the whya bit more aetiology risk
factors, you said T cell mediated, but what actually sets
that off? Yeah.
So the exact initial spark, still a bit of a mystery, but
(04:26):
the general idea is it's an autoimmune type response where
the immune system gets misdirected against the body's
own skin or mucosal cells. What might nudge it in that
direction? What are the potential triggers
or things that make it worse? Well, the source of point to a
few things. There might be a genetic
predisposition. Sometimes it runs in families.
Viral infections like we said, Hep C is the main one to flag
(04:48):
those medications. We listed beta blockers, NSAI,
thiazides, antimalarials, gold and potentially allergens.
Maybe contact allergens like dental materials for oral LP or
other environmental factors. So if we list the actual risk
factors explicitly, what makes someone more likely to get it?
OK. Based on that, definitely a
(05:09):
family history having certain infections, especially hepatitis
C, exposure to those known trigger medications and
potentially exposure to certain allergens or environmental
triggers. Makes sense.
So we have the what and the potential why?
Now the how. Let's talk pathophysiology.
What's actually happening at thecellular level to create those
(05:29):
lesions? Right, this is where those T
cells come in. It's primarily CD 8 + T cells, a
specific type of immune cell. These cells target the basal
keratinocytes. Basal, meaning the bottom layer,
the foundation of the epidermis.Exactly.
Think of it like the skins foundation layer.
These CD 8 + T cells seem to recognise something on those
basal cells as foreign or abnormal and they attack them.
(05:50):
This happens in the skin and in mucous membranes.
So the body's own security forceattacking its own building
blocks. That's a good way to think about
it, yeah. And that attack releases
inflammatory signals, cytokines,which then 'cause all the
inflammation and the changes we see, the redness, the swelling,
the cell damage that leads to the papules and plaques.
And the trigger for that initialattack is still the unknown
(06:13):
part. Often, yes, though genetic
factors and those environmental triggers likely play a role in
making someone susceptible or setting it off.
OK, that helps visualise it. And this ties in nicely with
Histology, right? Which is super important for
tricky cases and exams. If you biopsy one of these
lesions, what are the classic microscopic findings?
(06:33):
Absolutely crucial. So under the microscope you're
looking for a few key things. First, a sawtooth appearance of
the REIT ridges. That's where the epidermis dips
down into the dermis. It looks jagged, not smooth.
Thought to you, it's got it. Second, a dense band like
infiltrate of lymphocytes, mainly those T cells clustered
right underneath the epidermis along that junction band of.
Lymphocytes. 3rd signs of damageto that basal cell layer.
(06:56):
We call it vacuular alteration or degeneration.
Yeah, basically the cells being attacked.
Right damage at the base. And 4th you often see
hyperkeratosis, which is thickening of the top layer of
skin and hypergranulosis, thickening of the granular layer
just below that. And does that granular layer
thickening link to anything we see clinically?
It's thought to that thickened granular layer is believed to be
(07:18):
what causes the appearance of Wickham's Tria.
Those white lines. So thick granular layer
microscopically links to white lines clinically.
Nice connection. Anything else on the Histology
report? Yes.
Sometimes you'll see these little pink blobs called SAVAT
bodies which are dead keratinocytes and direct
immunofluorescence or DIF can behelpful too.
What does DI show? It often shows deposits of
(07:41):
immunoglobulins, particularly IGN and fibrinogen, in a shaggy
pattern along that dermal epidermal junction.
OK, so key Histology buzzwords, sawtooth root ridges, band like
lymphocytic infiltrate, basal cell damage, hydrogranulosis
linked to Stryi and maybe IGN onDIFSBBHI, something like that.
(08:01):
Whatever works for you, Mimonicsare definitely helpful here.
OK. Speaking of things that might
look similar, differential diagnosis, what else could
present like lichen planus and potentially trip you up?
Good question. Always need to consider the
mimics for skin lesions you think about psoriasis, eczema,
maybe like a simplex chronicus which is from chronic scratching
(08:22):
and definitely drug reactions, specifically lycanoid drug
eruptions. Which look very similar.
Almost identical sometimes. That's why the medication
history is so vital. If they started a new beta
blocker with Thiazide recently, that's a big clue right?
And in the mouth. Oral differentials include
thrush, oral Candidiasis, but remember that usually wipes off
other oral lycanoid reactions, maybe from dental fillings and
(08:45):
importantly leukoplachia which is another white patch but can
also be precancerous. So differentiating is key.
Biopsy is often needed for oral lesions if unsure.
OK. And just thinking broadly, any
other conditions that sometimes get confused with LP from the
wider list? Yeah, things like cutaneous
graft versus host disease in transplant patients can look
(09:05):
similar. Discoid lupus erythropasias can
sometimes present with lesions that mimic LP and lichen
sclerosis, especially on the generals can overlap or be
confused, so keep a broad mind if it's not textbook.
Definitely. OK, let's zoom out again to the
big picture epidemiology. How common is it?
Who gets it? We mentioned the UK prevalence
(09:26):
around one 2%. It's mostly a condition of
middle age. Think 30s to 60s typically.
Yeah, and male versus female. Overall pretty similar for skin
LP, but for oral like and plaintiffs specifically it does
seem to be a bit more common in women.
Maybe a global ratio around 1 to1.5 female to male?
Interesting. And those associations again
globally? Yeah, the link with hepatitis C
(09:47):
is seen worldwide and also associations with hepatitis B
and primary biliary cirrhosis are noted in wider studies.
OK, prevalent enough to see middle-aged adults, maybe
slightly more oral LP in women and those important liver
disease connections. Right?
Let's really nail the clinical features.
Now back in the room with the patient.
What absolutely must you recognise?
OK consolidation time, cutaneousLP, itchy, purple, vilacious,
(10:13):
polygonal flat topped papules and plaques.
Think wrists, forearms, lower legs, ankles but can be
anywhere. Look hard for Wickham.
Striate those fine white lines. Sometimes easier to see if you
put a drop of oil or water on the lesion.
Good tip. And remember, after they heal
they can leave brown marks post inflammatory hyperpigmentation,
(10:34):
especially in darker skin. OK.
And mucous membranes? How common again?
And what's the look? Super common for oral
involvement. Up to 50% of people with skin LP
have it and some only have oral LP.
Look inside the cheeks, glucose,mucosa, the tongue, gums.
You'll often see white Lacy patches.
Maybe Wickham's dry again? Are they always sore?
No, they can be asymptomatic butoften they are sore, especially
(10:55):
if they become erosive or ulcerated.
Looks like raw red areas, sometimes with white edges.
General involvement is similar. Can be very painful erosions.
How do you tell oral LP from Thresh quickly?
Thrush is usually creamy or maybe look like cottage cheese
and crucially it should wipe offleaving a red base.
Lake and Planus is usually flatter, lacier and doesn't wipe
off. Got it.
Nail and scalp. Quick recap.
(11:16):
Males in up to 10%. Look for longitudinal ridges,
thinning, splitting, maybe terradium where the cuticle goes
forward. Scalp.
Lincoln plantipolaris, Patchy hair loss, redness, scaling
around follicles leading to scarring.
Alopecia. Less common, but important not
to miss. OK, so key features rundown
itchy purple polygonal rash wrists, legs, flexors, genitals
(11:39):
Wickham striae look for them Oral involvement in 50% Check
the mouth potential nail and scalp changes Diagnosis often
clinical. Spot on and always factor in
risk factors, Hep C, stress, newmeds, allergies and think about
those lycanoid drug mimics. Perfect mini case time.
Let's say a 55 year old man presents with intensely itchy
(11:59):
purple bumps on his wrist. You see faint white lines.
He also mentions a sore patch inside his cheek when he eats
salty crisps. What's jumping out at you?
That's screaming like in plaintiffs.
You've got the Puritic violations, polygonal papules on
a classic site, wrists with Wickhamstrae, plus symptomatic
oral involvement. Textbook presentation.
Really. Excellent.
Now what if it's not so textbook?
(12:20):
What investigations might you actually order?
Well, if it looks classic, you often don't need investigations.
Diagnosis is clinical, but if it's atypical or you need to
rule out something more sinisterlike malignancy in an oral
lesion or differentiate from a mimic, then a biopsy is your go
to. A punch biopsy.
Usually, yes, a punch biopsy sent for histopathology and we
(12:43):
know what they're looking for. Sawtooth band like infiltrate,
basal damage, hypergranulosis. Exactly, and you might ask for
direct immunofluorescence DIF ona separate biopsy sample taken
from near lesion looking for those IGN deposits.
OK. Any other tests?
Well, for persistent oral LP, especially if you suspect a link
to amalgam fillings, patch testing could be considered to
(13:05):
look for contact allergy, right?And given the strong
association, definitely considerhepatitis C testing,
particularly if the oral LP is erosive or if the patient has
any risk factors for Hep C. So investigations mainly for
confirmation and tricky cases orchecking for associations like
hep C clinical picture is king usually, right?
Let's talk management. How do we actually help these
(13:26):
patients? It really depends.
For mild skin LP that isn't too bothersome it might resolve on
its own so just reassurance might be needed.
But if it's itchy, widespread, or affecting mucous membranes
causing symptoms, then treatmentis usually warranted.
First step if you suspect a drugtrigger.
Stop the drug. If it's a lycanoid drug
eruption, removing the trigger is the most important step and
(13:48):
can lead to resolution. OK.
For itchy skin lesions, what's the first line?
Potent or super potent topical corticosteroids.
That's the mainstay creams or ointments applied directly to
the lesions. How do they help?
They reduce the inflammation andtherefore the itch and help the
lesions clear faster. For really thick stubborn
lesions, hypertrophic LP, sometimes applying the steroid
(14:10):
under occlusion like cling film overnight can boost its effect.
Antihistamines can help with theitch symptomatically too.
And for the mouth, oral LP. Again, topical steroids are
first line for symptomatic oral LP.
These come as mouthwashes, sprays or pastes that stick to
the lining of the mouth. Things like benzi tapping,
mouthwash or spray can also helpsoothe soreness.
(14:31):
What if topicals aren't cutting it or the disease is really
widespread or severe? Then you need to step up to
systemic treatment. Often this means a course of
oral corticosteroids like Prednisolone, usually for
several weeks, then slowly tapered down.
Any other options beyond steroids?
Yes, for difficult or persistentcases.
Other options include immunosuppressants like
(14:52):
azathioprine or mycophenolitma. Fatal.
Sometimes oral retinoids like acetretin are used.
Hydroxychloroquine is another one mentioned and phototherapy.
Light treatment. Exactly.
Narrowband UVB or Puva Soarland plus UVA Light can be very
effective for widespread itchy cutaneous lichen planus that
(15:12):
hasn't responded well to topicals.
OK, so summarising management stop triggers if suspected first
line for skin oral is potent. Topical steroids maybe
intralesional steroids for thicklesions step up to oral
steroids, other immunosuppressants, retinoids or
phototherapy for severe widespread refractory disease.
Symptomatic relief with antihistamines or anaesthetic
(15:33):
mouthwashes. That's a pretty good overview of
the treatment ladder. Right quick MSRA scenario on
management. A patient has widespread, very
itchy cutaneous lichen planus. Potent topical steroids haven't
really worked after a good few weeks.
What might be a reasonable next step?
Given it's widespread and not responding to topicals, you'd
think about systemic options. So starting a course of oral
(15:55):
corticosteroids or referring forphototherapy like UVB or PUVA
would be appropriate next steps to consider.
Makes sense nearly there prognosis.
What's the long term outlook? It's quite variable honestly.
Skin licking plant is often doesburnout, maybe within one two
years, but it can recur. And the mouth and other mucous
membranes. They tend to be much more
chronic. Erosive oral or genital OBP can
(16:17):
grumble on for many years with flare ups and periods of
remission. It's less likely to resolve
completely on its own. And even when the active bits
clear up. You can be left with changes
that post inflammatory hyperpigmentation.
The brown marks can persist for a long time and scarring is a
real issue, especially with lichen plantiplearis on the
scalp causing permanent hair loss or severe erosive disease
(16:39):
potentially causing scarring in the mouth or genitals.
So follow up is often needed. Which brings us neatly to
complications. What are the main problems or
long term issues we need to be aware of?
OK, this is super important for oral and genital LP.
The main issues are pain, soreness, ulceration.
This can make eating, drinking, speaking or sexual activity
(17:01):
really difficult and impact quality of life massively.
Can even lead to weight loss if eating is tough.
And the really serious one. The risk of malignant
transformation, specifically oral squamous cell carcinoma.
OSCC developing within the long standing, particularly erosive
oral lichen planus lesions. What's the kind of risk level
we're talking? The figures quoted are around a
(17:22):
1.1% risk over time. It's not huge, but it's
significant enough that regular oral cheques are recommended for
these patients. And does anything increase that
risk further? Yes, smoking and coexisting
hepatitis C infection seem to significantly increase the risk
of OSCC development in patients with oral LP, which again
highlights why asking about smoking and considering Hep C
(17:44):
testing is so important. Wow, so that really underlines
the need for monitoring any other complications?
Well, the persistent hyperpigmentation can be
cosmetically bothersome and rarely carcinoma can develop in
chronic vulval like in planus lesions too.
And of course, the underlying association with Hep C itself is
a complication to manage. So it's a condition that might
(18:06):
seem like just a rash sometimes,but particularly the oral and
genital forms need careful management and long term
surveillance because of that small but real risk of cancer,
especially if they smoke or haveHep C.
Exactly, you absolutely must check the mouth, ask about
symptoms there, consider risk factors and arrange follow up.
Particularly for erosive disease, it's not just about
(18:26):
treating the itch on the skin. That's a really crucial takeaway
message, right? We've covered a lot of ground,
the definition, the T cell cause, the classic 6 PS and
Wickham Strea, the key Histologymanagement from topicals to
systemics and those vital complications like OSCC risk.
Hopefully this deep dive gives you a solid high yield overview
for Leakin Planus when it comes up in your MSRA revision.
(18:49):
Yeah, connecting the pathology to the presentation and hitting
those high yield points for the exam was the goal.
Absolutely. Well, thanks for joining us for
this deep dive into Leakin Planus.
For more free MSRA revision resources, visit freem-sra.com
and for the full Premium Revision Toolkit, head to pass
them ssra.com.
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